A 45-year-old hospitalized man is evaluated for worsening kidney function. The patient has a history of alcoholic cirrhosis and was admitted 3 days ago due to progressive abdominal pain and lethargy. Evaluation revealed asterixis and 300/mm³ of neutrophils in the ascitic fluid. He was started on intravenous cefotaxime and oral lactulose for treatment of spontaneous bacterial peritonitis complicated by hepatic encephalopathy. The patient's symptoms have gradually improved with treatment, but his serum creatinine has increased from 0.9 mg/dL on admission to 2.1 mg/dL now. Urine output during the last 24 hours is 450 mL. He has no history of kidney disease or other medical problems. The patient's home diuretic therapy with furosemide and spironolactone had been initially continued during the hospitalization but was stopped yesterday. He stopped drinking alcohol after being diagnosed with cirrhosis 3 years ago and does not use tobacco.
Temperature is 37.2 C (99 F) , blood pressure is 110/70 mm Hg, pulse is 96/min, and respirations are 18/min. The patient is somnolent but easily roused. There is mild scleral icterus, and jugular venous pressure is normal. Lungs are clear to auscultation. The abdomen is soft, moderately distended with ascites, and nontender. Bowel sounds are normoactive. There is 2+ bilateral lower-extremity pitting edema.
Laboratory results are as follows:
Renal ultrasonography shows no hydronephrosis.
Which of the following is the most appropriate next step in management of this patient's renal dysfunction?

Question

Quizplus · Accepted Answer

11ec193a_9720_a805_853d_03b31129714f_MD0002_00 This patient's advanced liver disease and rapidly developing acute kidney injury (AKI) raise suspicion for hepatorenal syndrome (HRS); spontaneous bacterial peritonitis (SBP) is a common precipitant of HRS. HRS likely results from increased activity of circulating vasodilators (eg, nitric oxide), leading to arterial vasodilation in the splanchnic and systemic circulation. The consequent decrease in renal perfusion pressure triggers compensatory renal vasoconstriction and marked reduction in glomerular filtration rate and urine production. HRS is largely a diagnosis of exclusion, which requires the following: Evidence of liver disease (usually cirrhosis) with portal hypertensionAKI in the absence of other causes (eg, shock, nephrotoxic agents)Urine red blood cells <50/hpf and urine protein <500 mg/dayLack of improvement in AKI after 48 hours of diuretic cessation and volume expansion with albumin Evidence of liver disease (usually cirrhosis) with portal hypertension AKI in the absence of other causes (eg, shock, nephrotoxic agents) Urine red blood cells <50/hpf and urine protein <500 mg/day Lack of improvement in AKI after 48 hours of diuretic cessation and volume expansion with albumin This patient requires a diagnostic trial of intravenous albumin. If there is no improvement in renal function, HRS is diagnosed, and midodrine (a selective alpha-1 adrenergic agonist) and octreotide (a somatostatin analogue that reduces splanchnic vasodilation) can be added to treatment. Alternately, norepinephrine may be used for patients in an intensive care unit. These therapies typically act as a temporizing measure until hepatic function might be restored (eg, liver transplantation, spontaneous recovery of acute liver failure). (Choice A) Antibiotic discontinuation is appropriate for suspected acute interstitial nephritis; however, the absence of white blood cells on urinalysis makes this unlikely. This patient should continue cefotaxime to ensure sufficient treatment of SBP. (Choice C) Large-volume paracentesis (LVP) should be considered for renal failure due to suspected abdominal compartment syndrome; however, this patient's soft abdomen makes the diagnosis unlikely. In addition, chronic ascites may protect against abdominal compartment syndrome due to changes in abdominal wall compliance. In this patient with suspected HRS, LVP may further decrease renal perfusion and should be avoided at this time. (Choice D) Restarting furosemide is likely to cause intravascular volume depletion and lead to worsening renal dysfunction. Diuretics do not cause HRS but should be held in suspected HRS to allow a chance for renal recovery. (Choice E) Transjugular intrahepatic portosystemic shunts (TIPS) may improve renal function in some patients with HRS. However, due to the risk of complications and often poor outcome despite the procedure, TIPS is generally considered a last resort for patients who fail medical management. In addition, this patient's Model for End-Stage Liver Disease (MELD) score of >18 predicts poor 3-month survival following TIPS. (MELD) Educational objective: Hepatorenal syndrome presents with renal dysfunction and bland urine sediment in patients with advanced liver disease and portal hypertension. A 48-hour trial of diuretic cessation and volume expansion with albumin is required for the diagnosis. __________ References: Hepatorenal syndrome: Current concepts related to diagnosis and management. (http://www.ncbi.nlm.nih.gov/pubmed/27236146) Hepatorenal syndrome: Update on diagnosis and treatment. (http://www.ncbi.nlm.nih.gov/pubmed/26558188) Diagnosis and management of acute kidney injury in patients with cirrhosis: Revised consensus recommendations of the International Club of Ascites. (http://www.ncbi.nlm.nih.gov/pubmed/25638527)

A 45-Year-Old Hospitalized Man Is Evaluated for Worsening Kidney Function